Pathogenesis (disease development)
Age-related wear and tear is not the cause of gonarthrosis; rather, acute damage to the articular cartilage from trauma or infection is usually at the beginning of joint destruction. Insufficient matrix synthesis and/or increased cell death of chondrocytes (cartilage cells) are discussed as pathogenetic mechanisms.The following pathomechanisms can be observed in gonarthrosis:
- Osteoarthritis due to excessive loading of the joint (repetitive microtrauma).
- Osteoarthritis due to inferior bone or cartilage.
Primary gonarthrosis occurs as a result of direct or indirect overloading of the joints.Direct overloading occurs during heavy work, sports* or due to obesity. Indirect overloads include a reduction in cartilage regeneration due to aging or metabolic disorders. * However, sport is only healthy as long as joints are not damaged in the process or as long as there are no pre-existing diseases.
Secondary gonarthrosis may occur as a result of:
- Congenital / malformation
- Malalignment (varus – valgus)
- Endocrinological disorders / diseases
- Metabolic disorders/diseases
- Inflammatory joint diseases
- Chronic inflammatory and non-inflammatory arthropathy (joint disease).
- Neurogenic diseases
- Rheumatic joint diseases
- Traumatic cartilage injuries
- Post-traumatic (after joint trauma/joint injury; dislocation – dislocation/dislocation).
- Operations
Osteoarthritis and inflammation (inflammation).
Low-grade inflammation seems to play a greater role in osteoarthritis (English osteoarthritis) than radiological changes in terms of osteoarthritis (signs of degeneration). This was shown by the determination of hs-CRP serum levels (high sensitivity CRP; inflammation parameter), which were slightly but statistically significantly increased compared to the control group.Clinically, about 50% of osteoarthritis patients show signs of synovial inflammation. The signs of synovitis (inflammation of the synovial membrane) are detectable even with minor symptoms and only limited structural changes. A typical immune cell infiltration with monocytes/macrophages and T lymphocytes (CD4 T cells) can be detected. Furthermore, cytokines (tumor necrosis factor-alpha (TNF-α); IFN-γ/interferon-gamma), growth factors and neuropeptides appear during this process. The mediators stimulate proinflammatory (“proinflammatory”) cytokines, among others.
Etiology (causes)
Biographic causes
- Genetic burden from parents, grandparents:
- z. E.g., through vitamin D receptor (VDR) gene polymorphisms.
- There were significant associations between VDR apal polymorphisms and osteoarthritis in the Asian population, but not in the overall population
- There was also a statistically significant association between FokI polymorphisms and osteoarthritis; however, this result was derived from only two studies
- Genetic diseases
- Ehlers-Danlos syndrome (EDS) – genetic disorders that are both autosomal dominant and autosomal recessive; heterogeneous group caused by a disorder of collagen synthesis; characterized by increased elasticity of the skin and unusual tearability of the same (habitus of the “rubber man”).
- Hemochromatosis (iron storage disease) – genetic disease with autosomal recessive inheritance with increased deposition of iron as a result of increased iron concentration in the blood with tissue damage.
- Marfan syndrome – genetic disease that can be inherited both autosomal-dominant or occur sporadically (as a new mutation); systemic connective tissue disease, which is notable primarily by tall stature, spider-limbedness and hyperextensibility of the joints; 75% of these patients have an aneurysm (pathological (pathological) bulge of the arterial wall).
- z. E.g., through vitamin D receptor (VDR) gene polymorphisms.
- Anatomical variants
- Congenital
- Joint axis displacement – e.g., scoliosis (S-shaped spine), pelvic tilt, knock knees (genu valgum), flat feet; leg length discrepancy (usually due to leg shortening).
- Knee malpositions (bow-leg position (genu varum), genu valgum, genu recurvatum, torsion defects, malformations of the patella/patella).
- Congenital
- Gender – Women suffer from gonarthrosis more frequently than men. A suspected cause is the hormonal changes during menopause
- Age – age-related cartilage degeneration due to decreased metabolic activity; most important predictive factor for the development of gonarthrosis.
- Occupations – occupations with long-lasting heavy physical loads (e.g. construction workers, esp. tilers; soccer players).
Behavioral causes
- Consumption of stimulants
- Alcohol – ≥ 20 glasses of beer/week lead to a significant increase in coxarthrosis (hip osteoarthritis) and gonarthrosis (knee osteoarthritis); individuals who drank 4 to 6 glasses of wine per week had a lower risk of gonarthrosis
- Tobacco (smoking) – nicotine abuse promotes loss of articular cartilage in the knee joint
- Physical activity
- Underloading of the cartilage:
- Lack of physical activity – since cartilage gets its micronutrients from the synovial fluid, it relies on the joint being moved for cartilage growth
- Nutritive damage (eg, long rest in a cast).
- Overloading of the cartilage:
- Competitive and high-performance sports (e.g., soccer players).
- Long-lasting heavy physical stress
- Underloading of the cartilage:
- Overweight (BMI ≥ 25; obesity) – leads to overuse of the joints.
Disease-related causes
- Arthropathies (joint diseases), inflammatory, rheumatic.
- Aseptic bone necrosis – collective term for necrosis (“cell death”) of bone that occurs in the absence of infection (“aseptic”) due to ischemia (reduced blood supply).
- Chronic arthropathy – a number of conditions can lead to secondary joint disease. Both inflammatory and non-inflammatory processes may play a role. Examples include joint changes in hyperuricemia (gout) – uric acid-related, diabetes mellitus – glucose-related, hemophilia (bleeding disorder) or leprosy.
- Endocrinological disorders/diseases.
- Acromegaly – endocrinological disorder caused by overproduction of growth hormone (somatotropic hormone (STH), somatotropin), with marked enlargement of the phalanges or acras, such as the hands, feet, lower jaw, chin, nose and eyebrow ridges.
- Hyperparathyroidism (parathyroid hyperfunction).
- Malalignment (varus – valgus)
- Coxa valga luxans – shallow socket formation.
- Subluxation (incomplete dislocation) – e.g. hip, knee.
- Growth disorders in the epiphyseal region (area of the growth plates): e.g. in adolescent soccer players due tochronic, asymmetrical overloading of the growth plates near the knee joint and the simultaneous pull of the posterior thigh muscles → development of bow legs (genu varum).
- Hemophilia (hemophilia).
- Metabolic disorders/diseases
- Chondrocalcinosis (synonym: pseudogout); gout-like disease of the joints caused by deposition of calcium pyrophosphate in cartilage and other tissues; leads, among other things, to joint degeneration (often of the knee joint); symptomatology resembles an acute gout attack
- Diabetes mellitus
- Gout (arthritis urica/uric acid-related joint inflammation or tophic gout)/hyperuricemia (elevation of uric acid levels in the blood)
- Hemochromatosis (iron storage disease).
- Metabolic syndrome – clinical name for the symptom combination obesity (overweight), hypertension (high blood pressure), elevated fasting glucose (fasting blood sugar) and fasting insulin serum levels (insulin resistance) and dyslipidemia (elevated VLDL triglycerides, lowered HDL cholesterol). Furthermore, a coagulation disorder (increased tendency to clotting), with an increased risk of thromboembolism is also often detectable
- Ochronosis – deposition of homogentisic acid in the skin, connective tissue and cartilage.
- Rickets (synonym: English disease) – disease of growing bone with impaired mineralization of bones and disorganization of growth plates in children.
- Paget’s disease – disease of the skeletal system with bone remodeling.
- Neurogenic diseases (neuromuscular dyscoordination, tabes dorsalis).
- Traumatic cartilage damage
- Meniscal injuries
- Cruciate ligament and collateral ligament injuries
- Ahlbäck’s disease – aseptic bone necrosis, i.e. not caused by infection.
- Post-traumatic (after joint trauma/joint injury; dislocation – dislocation/dislocation).
Laboratory diagnoses – laboratory parameters that are considered independent risk factors.
- Hyperuricemia (elevation of uric acid levels in the blood).
Operations
- Z. E.g. meniscus removal: the risk of osteoarthritis increases 20-fold after meniscus damage.